Effect of Corticosteroid Administration on Vasopressin-Induced Adrenocorticotropin Release in Man

Clayton, George W.; Librik, Leon; Horan, Anthony H.; Sussman, Leon N.

doi:10.1210/jcem-25-9-1156

Cited by 19 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The minimal effective dose of AVP in ovine cells, and the dose required for plateau responses, is in close agreement with the doses of CRF required for these effects in rat cells [29]. The demonstration that the response to AVP can be blocked by prior treatment with dexamethasone is not unique to this study; a previous clinical study showed that dexa methasone attenuated lysine vasopressin-induced increases in plasma 17-hydroxycorticosteroids [8].…”

Section: Discussionsupporting

confidence: 79%

“…Al though arginine vasopressin (AVP) had long been known as a stimulus of ACTH release both in humans [8,14, 18] and ani mals [6,7, 22], ovine-(o)CRF was subsequently shown to be a much more potent stimulus of ACTH release from the rat ante rior pituitary both in vitro [29] and in vivo [24]. However, recent evidence suggests that oCRF is less potent than either AVP and K+ in dispersed human anterior pituitary (AP) cells [15], or than AVP, mesotocin or vasotocin in dispersed duck pituitary cells [5].…”

mentioning

confidence: 99%

See 1 more Smart Citation

Arginine Vasopressin Is a Much More Potent Stimulus to ACTH Release from Ovine Anterior Pituitary Cells than Ovine Corticotropin-Releasing Factor

et al. 1989

View full text Add to dashboard Cite

Cultured rat and ovine anterior pituitary cells were treated with a range of doses (0.01–1,000 nM) of arginine vasopressin (AVP) and ovine corticotropin-releasing factor (CRF), alone or in combination, and medium and cell content of immunoreactive (ir-)ACTH determined. In rat cells, a dose-response curve to CRF was obtained, with a threshold dose of 0.1 nM; AVP was much less effective alone, but augmented CRF responses when administered with CRF. In ovine pituitary cells AVP markedly stimulated ACTH release in a dose-dependent fashion, and with a threshold of 0.1 nM; in contrast, CRF increased ACTH release over basal only at doses > 100 nM. In combination, subthreshold doses of AVP potentiated rat pituitary cell responses to CRF; addition of 1 nM of AVP to varying doses of CRF was more effective in terms of ACTH release than addition of 1 nM of CRF to increasing doses of AVP. In contrast, in ovine cells the addition of 1 nM CRF to increasing doses of AVP elicited a larger ACTH response than the addition of 1 nM AVP to increasing doses of CRF. Dexamethasone pretreatment (5 nM) for 48 h significantly decreased CRF potentiation of AVP-stimulated ACTH release in ovine cells. These studies confirm that CRF is a more potent stimulus of ACTH release than AVP in the rat, and establish that in contrast AVP is a much more potent stimulus of ACTH secretion than CRF in isolated ovine pituitary cells.

show abstract

Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 99%

Arginine Vasopressin Is a Much More Potent Stimulus to ACTH Release from Ovine Anterior Pituitary Cells than Ovine Corticotropin-Releasing Factor

et al. 1989

View full text Add to dashboard Cite

show abstract

“…The elevation of the threshold for ACTH release may explain the findings of Gwinup (36) or of Clayton et al (40) that dexamethasone at a dose of approximately 2 jug/100 g body wt-assuming 70 kg subjects-in humans suppressed the increase in plasma 17-hydroxycorticosteroids that otherwise followed intravenous injections of lysine vasopressin at approximately 6 to 15 mU/100 g body wt. ACTH release following this dose of vasopressin in the rat also would appear to be suppressed by dexamethasone (at 25 /xg/ 100 g body wt) as shown in Fig.…”

Section: Discussionmentioning

confidence: 89%

Site of Action of Vasopressin in Causing Corticotropin Release1

et al. 1966

View full text Add to dashboard Cite

The corticotropin-releasing properties of lysine vasopressin and that of a porcine pituitary extract were compared by means of injections into hypothalamic sites or into the adenohypophysis of dexamethasone-pretreated rats of both sexes. In all cases the doses used for central injections were below the minimal dose capable of causing an increase in adrenal secretion of corticosterone after intravenous injection, so that corticotropin (ACTH-like) effects or contamination by ACTH could be excluded as a cause of increased adrenal secretion of corticosterone after the central injections. Vasopressin provoked extensive release of ACTH when it was placed in the median eminence of the hypothalamus, as did the pituitary extract. When the 2 substances were tested by intra-adenohypophysial injection, the vasopressin caused much less ACTH release and the extract caused more ACTH release than observed after intrahypothalamic injections. Morphine abolished the ACTH release after vasopressin injections at either site, as well as after the injection of the extract into the median eminence. However, morphine failed to abolish, or even diminish extensively, the ACTH release observed after injection of the extract into the anterior pituitary. From these results it was concluded that the extract contained activity resembling that of a corticotropin-releasing factor, but that vasopressin did not have such activity at the doses used. The vasopressin apparently acted directly on the hypothalamus to cause release of endogenous corticotropin-releasing factor. (Endocrinology 79: 328, 1966)

show abstract

“…Since 1954, when McCann and Brobeck showed that vasopressin produces release of ACTH in rats with hypothalmic lesions, many successful experiments have been performed in which purified pos terior pituitary extract or synthetized vasopressin has been used to test the ACTH-producing potency of the human pituitary [McD onald et al, 1956[McD onald et al, , 1959Bernard-Weil et a/., 1956a, b, 1963a, b, 1967Clayton et al, 1957Clayton et al, , 1963Clayton et al, , 1965Linquette et al, 1959;Israels and de Wikd 1960; Wal et al, 1961Wal et al, , 1965Bariety et a/., 1963;Rappaport et al, 1963;D ecourt and Bernard-Weil, 1965;G winup, 1965,1967Landon et a!., 1965;Lundberg and W ide, 1966;Bethge et al, 1967;K nebusch, 1967;N ieman et al, 1967;Rinnk and N ordstrom, 1967;Silvestrini et al, 1967;Strott et al, 1967;Webb-Peploe et al, 1967;Brostoff et al, 1968;Czarny et al, 1968;J asani et a!., 1968;J enkins and E lse, 1968;Rinne, 1968], It is clear from these experiments that an intramuscular injection or an intra venous infusion of vasopressin produces a secretion of ACTH fol lowed by a significant increase of plasma cortisol. It has been sug gested that the vasopressin test when used in combination with the Metopirone test could be of value for differentiating between hypo thalamic and hypophyseal insufficiency.…”

mentioning

confidence: 99%